CALCIUM METABOLIC CHANGES AND CALBINDIN-D IN EXPERIMENTAL-HYPERTENSION

Objective: To examine renal and intestinal calbindin-D in relation to calcium metabolic changes in three different models of experimental hy pertension. Design: Spontaneously hypertensive rats (SHR), hypertensio n-prone Dahl salt-sensitive (Dahl-S) rats and the Goldblatt two-kidney , one clip rat model of renovascular hypertension were examined. Resul ts: Both prehypertensive and hypertensive SHR had significantly lower concentrations of both renal calbindin-D28k and intestinal calbindin-D 9k than Wistar control rats. This was accompanied by hypocalcaemia, hy pomagnesaemia and increased plasma 1,25(OH)(2) vitamin D levels. Induc tion of hypertension in Dahl-S rats reduced intestinal calbindin-D9k a nd increased plasma levels of 1,25(OH)2 vitamin D, while renal calbind in-D28k levels, plasma calcium levels and plasma magnesium levels were unchanged. Renovascular hypertension was associated with a significan t increase in the intestinal calbindin-D9k, plasma 1,25(OH)(2) vitamin D, parathyroid hormone and magnesium levels, while renal calbindin-D2 8k, plasma calcium and phosphorus levels were unaffected. Conclusions: These three models of experimental hypertension have clearly demonstr ated three separate patterns in the regulation of renal and intestinal calbindin-D, which relate to different alterations of factors involve d in calcium and magnesium metabolism. In all three models hypertensio n was accompanied by a significant increase in plasma concentrations o f 1,25(OH)(2) vitamin D. Only rats with renovascular hypertension show ed increased intestinal calbindin-D9k levels, whereas reduced concentr ations were found in the SHR and in the hypertensive Dahl-S rats. This indicates the existence of a resistance at the cellular level to 1,25 (OH)2 vitamin D affecting the expression of calbindin-D in both SHR an d Dahl-S rats.